Molecular structure explains how ‘arsenic life’ bacteria rely on phosphate instead
Hardy bacteria that live in an arsenic bath survive in part by keeping poison from entering their cells, scientists have found. Just one tiny tweak in a hydrogen bond is enough to let the microbes pick out the phosphate they need to build their DNA — while keeping the arsenic out.
The work helps explain how famous bacteria in the arsenic-rich waters of Mono Lake, Calif., manage to live there without incorporating arsenic into their DNA, as a controversial 2010 paper had claimed (SN: 2/25/12, p. 10).
“It goes to show that life will find a way,” says Matthew Pasek, a geochemist at the University of South Florida who was not involved in the new study.
The discovery may also open new ways to deliver substances into a cell that are wanted, like drugs, while keeping unwanted stuff out. “The best way of avoiding poison is not to take it, and this is like the first defense mechanism,” says Mikael Elias, a biochemist at the Weizmann Institute of Science in Rehovot, Israel. He and his colleagues describe the finding online October 3 in Nature.
Mono Lake contains a witch’s brew of chemicals, yet a strain of Halomonas bacteria somehow manages to thrive there. The original “arsenic life” paper contended that the strain took up arsenate (a combination of arsenic and oxygen) in place of phosphate, the structurally similar chemical that forms the backbone of DNA in living organisms.
Elias had been studying the class of proteins that cells use to pull in phosphate, and suspected that Halomonas somehow fishes out the tiny bits of phosphate available from a sea of arsenate. So he and his colleagues examined the structures of five proteins, including two from the Mono Lake strain of Halomonas, that pull phosphate from the environment into cells.
All the proteins contain a particular hydrogen bond that latches onto phosphate (and arsenate). But structurally, that bond is slightly different in the Halomonas protein thought to be most responsible for choosing phosphate over arsenate. “It’s really a tiny difference, but it has a big consequence,” says Elias. “Basically with phosphate this bond is almost perfect” — but with the slightly larger arsenate the bond is much harder to make. That difference lets Halomonas take up phosphate molecules about 4,500 times as efficiently as it takes up arsenate, the team found. The other proteins tested all pick out phosphate over arsenate, but not nearly as dramatically.
Other structurally similar molecules, such as one based on vanadium, also compete with phosphate for getting into cells, says Pasek. The new work might help explain the great evolutionary mystery of why phosphate usually triumphs.
The original arsenic-life paper reported that the Halomonas strain grew in the presence of arsenate alone. But some tiny amount of phosphate must have been present in that mix, scientists suspect.
“The new results add to the growing evidence that the earlier claim … was indeed incorrect,” says Tony Hunter, a biologist at the Salk Institute for Biological Studies in La Jolla, Calif.
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